Neuromuscular junction dysfunction in Miller Fisher syndrome.
Autor(es): Silverstein M. P.; Zimnowodzki S.; Rucker J. C.
Resumo: The Miller Fisher syndrome (MFS) is a variant of Guillain-Barre syndrome with the clinical triad of areflexia, ataxia, and ophthalmoparesis. The classic pathologic mechanism of disease is considered to be peripheral nerve demyelination. We present a patient with binocular diplopia and a diagnosis of myasthenia gravis from 15 years prior. Electrophysiologic studies revealed a decremental response on repetitive nerve stimulation, suggesting recurrent myasthenia. However, pupillary light-near dissociation and areflexia were present and positive anti-GQ1b antibodies confirmed MFS. This patient highlights a developing recognition of impaired neuromuscular transmission in MFS. His presentation is discussed in the context of the animal and human literature on neuromuscular junction abnormalities in MFS.
Imprenta: Seminars in Ophthalmology, v. 23, n. 3, p. 211-213, 2008
Identificador do objeto digital: 10.1080/08820530802049996
Descritores: Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies ; Guillain-Barre Syndrome - Transmission ; Guillain-Barre Syndrome - Immunology
Data de publicação: 2008
